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Fangchinoline accumulates autophagosomes by inhibiting autophagic degradation and promoting TFEB nuclear translocation
Tang, Zheng-Hai; Guo, Xia; Cao, Wen-Xiang; Chen, Xiuping; Lu, Jin-Jian
2017
Source PublicationRSC ADVANCES
ISSN2046-2069
Volume7Issue:67Pages:42597-42605
Abstract

Autophagy, an evolutionarily conserved cellular self-digestive process, is associated with different diseases and can be inhibited or induced by a series of agents. In this study, we reported that fangchinoline (FCL), an alkaloid from Stephania tetrandra S. Moore, increased the expression of LC3-II and the formation of GFPLC3 puncta in non-small cell lung cancer (NSCLC) cells. Numerous yellow puncta were observed in mRFPEGFP- LC3 stably expressed NSCLC cells under FCL treatment and the FCL-increased expression of LC3-II was not further increased after co-treatment with bafilomycin A1, an autophagy inhibitor, suggesting that FCL inhibits autophagic flux. Results of co-localization of GFP-LC3 with LysoTracker Red or lysosomal-associated membrane protein 1 indicated that FCL inhibits autophagosomes-lysosomes fusion. Furthermore, FCL decreased the activities of cathepsin B and cathepsin D and affected the cellular acidification. Interestingly, FCL also increased the nuclear translocation of transcription factor EB (TFEB), a master regulator of autophagic and lysosomal genes, and the mRNA expressions of TFEB-targeted genes, such as SQSTM1, MAP1LC3B, and UVRAG. Knockdown of TFEB by using small inference RNA decreased the FCL-induced expression of LC3-II and the formation of GFP-LC3 puncta. Overall, we reported that FCL increases the expressions of autophagy markers via both inhibition (inhibition of autophagosomes-lysosomes fusion and dysfunction of lysosome) and induction (promotion of TFEB nuclear translocation) of autophagy, providing insights into the better understanding of the complexity of agent-mediated autophagy.

DOI10.1039/c7ra02738a
URLView the original
Indexed BySCI
Language英语
WOS Research AreaChemistry
WOS SubjectChemistry, Multidisciplinary
WOS IDWOS:000409147500073
PublisherROYAL SOC CHEMISTRY
The Source to ArticleWOS
Fulltext Access
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Cited Times [WOS]:1   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionInstitute of Chinese Medical Sciences
AffiliationState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, 7014, N22, Avenida da Universidade, Taipa, Macao, China
First Author AffilicationInstitute of Chinese Medical Sciences
Recommended Citation
GB/T 7714
Tang, Zheng-Hai,Guo, Xia,Cao, Wen-Xiang,et al. Fangchinoline accumulates autophagosomes by inhibiting autophagic degradation and promoting TFEB nuclear translocation[J]. RSC ADVANCES,2017,7(67):42597-42605.
APA Tang, Zheng-Hai,Guo, Xia,Cao, Wen-Xiang,Chen, Xiuping,&Lu, Jin-Jian.(2017).Fangchinoline accumulates autophagosomes by inhibiting autophagic degradation and promoting TFEB nuclear translocation.RSC ADVANCES,7(67),42597-42605.
MLA Tang, Zheng-Hai,et al."Fangchinoline accumulates autophagosomes by inhibiting autophagic degradation and promoting TFEB nuclear translocation".RSC ADVANCES 7.67(2017):42597-42605.
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